Specific SLE-factors are also hypothesised to play a role,4 with reported associations between autoantibodies and CD, particularly anti-N-methyl-D-asparate, anti-dsDNA and antiphospholipid (aPL) antibodies.5 Structural brain alterations in SLE such as cerebrovascular events, and the increased number of white matter hyperintensities6 also may contribute, although others have suggested that such structural changes are not directly associated with CD. The gene discussed is FASLG; the disease is systemic lupus erythematosus.